Acute exposure of a severe stressor can result in analgesia. Repeated exposures result in a progressive decline of the analgesic response, in much the same manner that the pituitary-adrenal repsonses to stress show adaptation. Virtually every physical stressor increases plasma levels of Beta-endorphin as well as ACTH and corticosterone; however, not all stressors produce analgesia. Some stressors induce an analgesic response that is sensitive to opiate receptor blockade by naloxone, others cause a non-naloxone sensitive analgesia. The proposed set of psychophysical experiments will assess whether the sensory changes induced by various stressors are specific tothe modality of pain or whether they are accompanied by deficits n auditory and/or visual acuity as well. A new reflex inhibition psychophysical technique, based upon the startle response, will be employed to circumvent the confounding effects of stress upon the performance aspects of traditional operant sensory discrimination techniques. An interlocking set of experiments will also determine whether opioid and non-opioid forms of stress-induced analgesia differ in their sensory correlates and, consequently, whether either or both reflects a tur analgesic state. In turn these data will gear on whether the various forms of stress-induced analgesia may be counted as evidence for the existence of more than one intrinsic pain-inhibitory system.